霍奇金淋巴瘤（HL）是一种淋巴肿瘤，通常见于颈部淋巴结。该疾病是多因素影响的，近年来，血管生物学领域对各种血管分子之间的关系进行了探索。血管生物学与 HL 之间的联系错综复杂，且若干途径的作用仍不清楚。本综述总结了血管生物学与 HL 之间的细胞和分子关系。与血管生物学各种功能相关的蛋白质，包括细胞因子（TNF-α、IL-1、IL-13 和 IL-21）、趋化因子（CXCL10、CXCL12 和 CCL21）、粘附分子（ELAM-1/VCAM-1） ）和生长因子（BDNF/NT-3、血小板源性生长因子受体-α）已与肿瘤活性相关。值得注意的肿瘤活性包括诱导 NF-kB 依赖性途径的旁分泌激活、粘附分子调节的上调、基因组扩增以及 MHC-II 介导的抗原呈递的有效丧失。临床前研究模型（主要是使用细胞培养的模型）已针对 HL 进行了优化。动物模型，特别是小鼠，也被用作复杂生物系统的替代品，研究主要集中在疾病的生理病理学评估上。这些生物分子值得进一步研究，因为它们可能揭示模糊的途径并作为预防和/或治疗干预的目标。

Hodgkin's lymphoma (HL) is a lymphatic neoplasm typically found in the cervical lymph nodes. The disease is multifactorial, and in recent years, the relationships between various vascular molecules have been explored in the field of vascular biology. The connection between vascular biology and HL is intricate and the roles of several pathways remain unclear. This review summarizes the cellular and molecular relationships between vascular biology and HL. Proteins associated with various functions in vascular biology, including cytokines (TNF-α, IL-1, IL-13, and IL-21), chemokines (CXCL10, CXCL12, and CCL21), adhesion molecules (ELAM-1/VCAM-1), and growth factors (BDNF/NT-3, platelet-derived growth factor receptor-α), have been linked to tumor activity. Notable tumor activities include the induction of paracrine activation of NF-kB-dependent pathways, upregulation of adhesion molecule regulation, genome amplification, and effective loss of antigen presentation mediated by MHC-II. Preclinical study models, primarily those using cell culture, have been optimized for HL. Animal models, particularly mice, are also used as alternatives to complex biological systems, with studies primarily focusing on the physiopathogenic evaluation of the disease. These biomolecules warrant further study because they may shed light on obscure pathways and serve as targets for prevention and/or treatment interventions.